Metastasis and paclitaxel (PTX) resistance are the main reason for the poor prognosis of ovarian cancer (OC).Evidence showed that RNA-binding proteins (RBPs) and long noncoding RNAs (lncRNAs) can modulate posttranscriptional regulation. The aim of this study was to determine the relationship among RBP, lncRNA and OC and to further guide clinical therapy. Immunohistochemistry revealed that pre-mRNA processing factor 6 (PRPF6) was upregulated in OC chemoresistant tissues and was closely related to advanced (Federation of International of Gynecologists and Obstetricians) FIGO stages and chemo-resistance. PRPF6 promoted progression, and PTX resistance in vitro and in vivo. And the transcripts of small nucleolar RNA host gene SNHG16-L/S were differentially expressed in OC cells and tissues as detected through real-time PCR (RT-PCR). SNHG16-L/S had opposite effects on progression and PTX resistance in OC. Mechanistically, SNHG16-L inhibited GATA-binding protein 3 (GATA3) transcription by binding to CCAAT/enhancer-binding protein B (CEBPB). Moreover, PRPF6 induced the alternative splicing of SNHG16, causing downregulation of SNHG16-L and, leading to the upregulation of GATA3 expression to further promote metastasis and PTX-resistance in OC. Totally, these data unveiled that PRPF6 promotes metastasis and PTX resistance of OC through SNHG16-L/CEBPB/GATA3 axis, which provides a new direction for OC treatment.

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Background: Metastasis and paclitaxel (PTX) resistance are the main reason for the poor prognosis of ovarian cancer (OC). Evidence has shown that RNA-binding proteins (RBPs) and long noncoding RNAs (lncRNAs) can modulate post-transcriptional regulation. The aim of this study was to determine the relationship among RBP, lncRNA and OC and to further guide clinical therapy. Methods: The expression of pre‐mRNA processing factor 6 (PRPF6) in OC tissues form 68 patients were detected by Immunohistochemistry. The expression of small nucleolar RNA host gene 16(SNHG16) transcripts-SNHG16-L/S in OC cell lines were analyzed by real-time PCR (RT-PCR). Transwell, CCK8 assays and flow cytometry analyses were used to detected effects of PRPF6 and SNHG16 on tumorigenesis and PTX-resistance. Molecular interactions were examined by dual‐luciferase reporter gene assay, RNA immunoprecipitation and chromatin immunoprecipitation. OC cells that knockdown PRPF6 were injected subcutaneously in nude mice.Results: The results showed that PRPF6 was upregulated in OC chemoresistant tissues and was closely related to advanced FIGO stages. PRPF6 promoted progression, and PTX resistance in vitro and in vivo. SNHG16-L/S were differentially expressed in OC cells and tissues as detected through real-time PCR (RT-PCR). SNHG16-L/S had opposite effects on progression and PTX resistance in OC. Mechanistically, SNHG16-L inhibited GATA-binding protein 3 (GATA3) transcription by binding to CCAAT/enhancer-binding protein B (CEBPB). Moreover, PRPF6 induced the alternative splicing of SNHG16, causing downregulation of SNHG16-L and, leading to the upregulation of GATA3 expression to further promote metastasis and PTX-resistance in OC.Conclusions: Totally, these data unveiled that PRPF6 promotes metastasis and PTX resistance of OC through SNHG16-L/CEBPB/GATA3 axis, which provides a new direction for OC treatment.

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